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E‐cadherin‐mediated contact of endothelial progenitor cells with mesenchymal stem cells through β‐catenin signaling
Author(s) -
Xia Jie,
Zhang Hongwei,
Gao Xiaopeng,
Guo Jun,
Hou Jixue,
Wang Xiaoyi,
Wang Sibo,
Yang Tao,
Zhang Xuyong,
Ge Quanhu,
Wan Longfei,
Cheng Wenzhe,
Zheng Jinpo,
Chen Xueling,
Wu Xiangwei
Publication year - 2016
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1002/cbin.10579
Subject(s) - mesenchymal stem cell , microbiology and biotechnology , progenitor cell , angiogenesis , catenin , cadherin , stem cell , beta catenin , cell adhesion , chemistry , biology , adhesion , cancer research , signal transduction , cell , wnt signaling pathway , biochemistry , organic chemistry
Mesenchymal stem cells (MSCs) and endothelial progenitor cells (EPCs) are attached to each other in the bone marrow (BM) cavity and in in vitro cultures, and this adhesion has important physiological significance. We demonstrated that cell proliferation could be promoted when MSCs were co‐cultured with EPCs, which was beneficial to angiogenesis, tissue repair, and regeneration. The adhesion of MSCs and EPCs could promote the pluripotency of MSCs, particularly self‐renewal and multi‐differentiation to osteoblasts, chondrocytes, and adipocytes. This study focused on the mechanism of adhesion between EPCs and MSCs. The results showed that E‐cadherin (E‐cad) mediated the adhesion of MSCs and EPCs through the E‐cad/beta‐catenin signaling pathway. The E‐cad of EPCs occupied a dominant position during this process, which activated and up‐regulated the beta‐catenin (β‐catenin) of MSCs to improve cohesion and exert their biological function.